Introduction to TPN

新光吳火獅紀念醫院 內科部 胃腸肝膽科

柯威旭 醫師

Nutrition Support Team

• Physicians• Clinical pharmacists• Nurse-Clinicians• Dietitians• Laboratory research technician• Ward nursing staff• In SKH: 主任 ,執行秘書 ,各科醫師 ,藥劑師 ,營養師

Source of Nutrition

• Enteral nutrition

• Parenteral nutrition– Central parenteral nutrition (CPN=TPN)– Peripheral parenteral nutrition (PPN)– Long-term home parenteral nutrition (HPN)

Clinical decision algorithm route of nutrition support

Decision to institute special nutrition support

Oral Feeding

Nutrition Assessment

Functional GI Tract

Enteral Nutrition Parenteral Nutrition

GI function PPN TPN

GI function returnIntactNutrients

DefinedFormula

Adequate InadequatePN

Short-term: NG, ND,NJ

Long-term:Gastrostomy Jejunostomy

YES NO

NOYESAdequate

PPN

• High risk of thrombophlebitis• Osmolarity: less than 800-900 mOsm/kg• Short-term: up to 2 weeks• Not the optimal choice for

– significant malnutrition– severe metabolic stress– large nutrient or electrolyte needs (especially potassium,

a strong vascular irritant)– fluid restriction– the need for prolonged intravenous nutrition support

Indications of TPN

• Impossibility for enteral nutrition

• Inadequacy for enteral nutrition

• Increment of the severity of disease by enteral nutrition

PLUS

• Anticipated to have PN for more than 7 days

TPN in Internal Medicine• Acute pancreatitis• Intestinal disease (IBD, NEC, radiation colitis, ileus, int

ractable diarrhea / vomiting)• Cancer• Hepatic failure• Renal failure• Short bowel syndrome• Enterocutaneous fistula• AIDS• Perioperative support

TPN should not be used in

• Malignancy: poor response to R/T or C/T

• Active stage of IBD

• Relative preserved GI function

• Hypertriglyceridemia (TG > 400 md/dl)

Components of TPN

• Carbohydrate, Amino acid, Fat, Electrolyte, Water, Vitamin, Trace element

• Standard solution– Dextrose, Amino acid– Electrolyte (Na, K, Cl, Mg, Ca, P)– Vitamin (A, B1, B2, Niacin, B6, Panthothenic a

cid, C, D, E, Zn, Cu, Mn, Cr)

• Lipid emulsion

Dextrose-content Solution

• 1 g glucose = 3.4 Kcal

• 1 g glucose = 5 mOsm/L

Amino acid solution

7% A.A.含 essential A.A. 較高 , 適用於腎衰竭病患

8% A.A.含高濃度 branch chain A.A., 低濃度 aromatic A.A., 可使肝衰竭病患之 HE 改善

12% A.A. 成人 Standard Solution 之 A.A. 來源

Lipid emulsions

10% intralipid

20% intralipid

10% lipofundin

Volume 500 ml/B 250 ml/B 100 ml/B

Calorie 550 Kcal/B 500 Kcal/B 110 Kcal/B

TPN formula

• B: standard solution• D: 8% A.A., high BCAA, low AAA; for

hepatic disease• E: 35% Dextrose, 12% A.A.; for HD and

water restriction• F: 29% Dextrose, 12% & 7% A.A.; for

ARF with HD• G: 29% Dextrose, 7% A.A.; for ESRD

TPN Order

Vascular Access for TPN

Care Complication Infection

Subclavian vein Easy High Low

Internal jugular vein Hard Low High

Femoral vein Hard Low Highest

Antecubital vein Easy Low High

Mechanical complication

• Insertion-of-catheter related:– pneumothorax, brachial plexus injury, subclavi

an and carotid artery puncture, hemothorax, thoracic duct injury and chylothorax, cardiac perforation, catheter malposition

• Air embolism

• Catheter fragment embolism

Metabolic complication• Fluid overload / Dehydration from osmotic diuresis• Hypertriglyceridemia• Hypocalcemia• Hypomagnesemia• Hypophosphatemia• Hyperglycemia / Rebound hypoglycemia on sudden

cessation of TPN• Hyperammonemia• Hyperchloremic metabolic acidosis• NKHS

Infectious complication

• Catheter-related sepsis: Staph. epidermidis and aureus; solution contamination

• GNB for immunocompromise• Direct evidence: tip culture or blood culture• Indirect evidence: fever (up to 38C, 2 times,

every 4 hours), chills, abrupt increase of blood sugar, hypotension, tachycardia, leukocytosis

Hepatic complication

• Biochemical: elevated serum aminotransferase and alkaline phosphatase

• Histological: steatosis, steatohepatitis, cholestasis, fibrosis and cirrhosis

• Usually benign and transient, but severe in TPN for > 16 weeks

• Additive use of Choline, Glutamine and Carnitine may be helpful

• If cholestasis is present, Cu and Mg should be deleted to prevent acculumation in liver and BG

Biliary complication

• Acalculous cholecystitis, GB sludge, cholelithiasis in TPN for > 3 weeks

• Decrease of bile salt reabsorption leads to formation of GB stone;

• Encouraging enteral intake to stimulate GB contraction

Intestinal complication

• Villous atrophy: decreases in gut weight and mucosal height

Metabolic bone disease

• Present in TPN for > 3 months

• Bone pain, bone fracture or asymptomatic but demineralization in CxR

• Possible mechanisms– Aluminum toxicity– Vitamin D toxicity– Negative calcium balance

Refeeding syndrome

• The metabolic and physiologic consequences of the depletion, repletion, compartmental shifts and interrelationships of the followings

– Phosphorus (< 1mg/dl, death within hours)– Potassium– Magnesium– Glucose metabolism– Vitamin deficiency– Fluid resuscitation

Case History• 66 y/o female, abdominal pain and anorexia

for 6 weeks

• persistent profuse, yellow, watery diarrhea after construction an ileal conduit for ureteral obstruction lasting for 3 months

• PE: BW 36 kg, 70% of IBW; afebrile, 108, 14, 98/70

anasarca, cachectic with generalized muscle wastage

Hct 38%, WBC 17000, BUN/Cr 22/1.0, K 3.4, P 3.4, HCO3 17, Sugar 48, Alb. 1.59

• Hospital Course TPN was started with 750g dextrose, 120g

AA, 60 mEq Na, 20 mEq K, 15 mmol P in 3L fluid

24 hrs after start of TPN, HR 180, SBP 50, CVP < 3 cmH2O

P 0.7, Na 142, K 1.4, HCO3 19, Mg 1.8, Sugar 1010, BUN/Cr 27/1.3 pH 7.31, O2 59, CO2 24 (O2 2L)

Apnea and respiratory failure developed within one hour

With stopping TPN and fluid replacement, P 6.9, K 3.5 and Sugar 45 were obtained.

In the following hospitalization, bilateral pneumonia and ARDS were complicated.

Died on the 6th day

• Autopsy: ischemic enterocolitis, pneumonia, ARDS and peritonitis and the heart was unremarkable

Sequence of events

P, Sugar, K, Meta. acidosis GI bleeding, Sepsis

Tachycardia, Hypotension

Apnea, MV support

ARDS, Pneumonia

Persistent Cardiopulmonary Instability

Death

Within 48 hrs of starting TPN After correction of hypophosphatemia

Physiology of Starvation

• When BMR = energy output to the limited intake, endogenous fuels must be used

• Major storage fuel is fat in form of TG (60-75 days)

• Carbohydrate, in contrast, is quantitatively insignificant storage fuel (1200 kcal, 1 day’s resting ER)

• Protein, 12kg, 2 weeks’ worth of calories; but is for nonfuel function

Metabolic Response to Refeeding

• A shift from body fat to CHO as major fuel source• Insulin • Glycogenolysis, gluconeogenesis and FA mobiliza

tion from adipose tissue is inhibited• Cellular uptake of glucose, K, P, and Mg is enhanc

ed by insulin• Antinatriuretic effect (Na retention and ECF expan

sion)

Patient of risk for refeeding syndrome

• Chronic alcoholism• Anorexia nervosa• Classic marasmus• Classic kwashiorkor• Chronic undernourishment• Morbid obesity with massive weight loss• Prolonged hypocaloric intravenous hydration• NPO for greater than 7-10 days• Cardiac and cancer cachexia

Recommendations to avoid refeeding syndrome

• Be aware of the syndrome• Recognize the patient at risk• Correct electrolyte

imbalance before initiating nutritional support whether by the oral , enteral or parenteral route

• Judiciously restore circulatory volume, monitor HR, and I/O

• Increase caloric delivery slowly

• Administer vitamins routinely

• Closely monitor electrolyte over the 1st week: Serum P, K, Mg, Sugar and urine electrolytes

• A little nutrition support is good, too much is lethal